BackgroundAntibiotic-associated diarrhea (AAD) is a risk factor for exacerbating the outcome of critically ill patients. Dysbiosis induced by the exposure to antibiotics reveals the potential therapeutic role of fecal microbiota transplantation (FMT) in these patients. Herein, we aimed to evaluate the safety and potential benefit of rescue FMT for AAD in critically ill patients.MethodsA series of critically ill patients with AAD received rescue FMT from Chinese fmtBank, from September 2015 to February 2019. Adverse events (AEs) and rescue FMT success which focused on the improvement of abdominal symptoms and post-ICU survival rate during a minimum of 12 weeks follow-up were assessed.ResultsTwenty critically ill patients with AAD underwent rescue FMT, and 18 of them were included for analysis. The mean of Acute Physiology and Chronic Health Evaluation (APACHE) II scores at intensive care unit (ICU) admission was 21.7 ± 8.3 (range 11–37). Thirteen patients received FMT through nasojejunal tube, four through gastroscopy, and one through enema. Patients were treated with four (4.2 ± 2.1, range 2–9) types of antibiotics before and during the onset of AAD. 38.9% (7/18) of patients had FMT-related AEs during follow-up, including increased diarrhea frequency, abdominal pain, increased serum amylase, and fever. Eight deaths unrelated to FMT occurred during follow-up. One hundred percent (2/2) of abdominal pain, 86.7% (13/15) of diarrhea, 69.2% (9/13) of abdominal distention, and 50% (1/2) of hematochezia were improved after FMT. 44.4% (8/18) of patients recovered from abdominal symptoms without recurrence and survived for a minimum of 12 weeks after being discharged from ICU.ConclusionIn this case series studying the use of FMT in critically ill patients with AAD, good clinical outcomes without infectious complications were observed. These findings could potentially encourage researchers to set up new clinical trials that will provide more insight into the potential benefit and safety of the procedure in the ICU.Trial registrationClinicalTrials.gov, Number NCT03895593. Registered 29 March 2019 (retrospectively registered).
Background
Sun’s procedure is currently recognized as the standard procedure for acute type A aortic dissection (AAAD). But the operation istoo difficult for beginners. We hope to reduce the difficulty and complications of this operation.
Methods
The aortic arch was immediately cross-clamped after the stented graft was inserted into the distal aorta. Thereafter, the lower-body perfusion was restored. Then, anastomosis was performed between the proximal stent graft and the distal 4-branched Dacron graft. The other arteries were anastomosed to the arched branch of the 4-branched graft.
Results
The cardiopulmonary bypass (CPB) time was (207 ± 52) min, and the aortic cross-clamp time was (114 ± 39) min. The circulatory arrest time was (38 ± 16) sec. One patient (4%) died. The incidence of complications was stroke (4%), renal dysfunction requiring dialysis (4%), prolonged intubation(12%).
Conclusions
The time of circulatory arrest in this operation is less than 1 min, which can avoid the complications caused by DHCA and decrease risk of bleeding and complexity by shifting anastomosis more proximally. The effect of our operation is similar to and even better than that of Sun’s procedure. It does not even require relatively advanced skill, much experience and excellent psychological quality, especially suitable for beginners.
The pro-survival transcription factor myocyte enhancer factor 2D (MEF2D) is identified to exhibit pro-tumor effects based on clinical and experimental studies. However, the detailed mechanisms underlying IGF-1-MEF2D pathway-induced tumor biology in cardiac myxoma (CM) was not clear. Here, we investigated the role of MEF2D in CM tissues and cells using RT-PCR, western blot, gene silencing, et al. Our findings revealed MEF2D was significantly increased in CM tissues compared with adjacent normal tissues and closely related to tumor size. In vitro assay demonstrated that IGF-1 enhanced CM cell proliferation in a time-dependent fashion. However, knockdown of MEF2D reversed the IGF-1-induced proliferative effects on CM cells in a time-dependent fashion and further resulted in cell cycle arrest. Based on the molecular level, IGF-1 enhanced the expression of epidermal growth factor receptor (EGFR) and matrix metalloprotein 9 (MMP9) in CM cells, whereas knockdown of MEF2D was able to reduce the expression of EGFR and MMP9 compared with vector control. Furthermore, we found knockdown of MEF2D directly affected G1/S transition in cultured CM cells. In conclusion, MEF2D regulates IGF-1-induced proliferation and apoptosis in CM development, indicating IGF-1-MEF2D pathway may be a useful target for treatment.
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